Action Points

There was a significant association between heightened cortisol response to mental stress and detectable plasma levels of cardiac troponin T using high-sensitivity assays in healthy participants, a finding which was independent of the presence of coronary atherosclerosis.

An elevated cortisol response to mental stress was linked to higher cardiac troponin T levels, suggesting that cortisol over-reactivity might explain why some people are more likely to develop heart disease, according to U.K. investigators.

A study of 508 healthy men and women between ages 53 and 76 found "a robust association between cortisol response and detectable high sensitivity cardiac troponin T (HS-CTnT)," a measure of cardiac cellular damage (OR 3.83; 95% CI 1.86-7.90; P<0.001), according to Antonio I. Lazzarino, MD, of University College London, and colleagues.

The association continued to exist even after multiple logistic regression analysis in which the investigators took into account several demographic variables and well-known cardiovascular risk factors that might contribute to the elevated troponin levels, they reported online in Journal of the American College of Cardiology. It even remained significant after the analysis factored in coronary calcification -- a marker for pre-clinical coronary atherosclerosis.

Over the years, several studies have found a strong link between mental stress and cardiovascular disease, the authors noted in their introduction. That research has shown that stress activates corticotrophin-releasing factor and arginine vasopressin neurons in the hypothalamus, which, in turn, cause the pituitary to release adrenocorticotropic hormone. That, in turn, causes the adrenal glands to release cortisol.

In addition, population studies have suggested a link between cortisol and subclinical atherosclerosis.

The current study involved participants chosen from the Whitehall II epidemiological cohort for psychophysiological testing between 2006 and 2008. Entry criteria included no history or objective signs of clinical or subclinical cardiovascular disease and no previous diagnosis or treatment for hypertension, inflammatory diseases, allergies, or kidney disease.

All study participants were white, and 56.5% were in full-time employment. Participants were subjected to a standardized mental stress test while having their salivary cortisol levels measured.

In light of these results, "further research is needed to understand the role of psychosocial stress in the pathophysiology of cardiac cell damage," the authors concluded.

One limitation they noted was that the study was cross-sectional "and therefore we cannot determine the causal sequence."

The study raises some difficult questions, Kai M. Eggers, MD, PhD, of Uppsala University in Sweden, wrote in an accompanying editorial. "What shall we do about this? Shall we simply recommend our patients (and their doctors) to go out, play in the sunshine and be happy? And try not to get stressed?" he wrote.

Instead, he suggested, "We can help our patients to cope with negative stress-related effects by referring them to psychosocial intervention programs -- an important but likely underused treatment option."

Eggers also noted that the stress-induced changes in cardiac troponin levels were the result of short-term exposure to a stress test, and added, "further studies are now warranted to investigate whether also chronic stressors (e.g., low social support, job stress and exhaustion, racial discrimination) would result in similar findings."

This research was supported by the British Heart Foundation and the Medical Research Council, U.K.

The researchers reported no conflicts of interest.

Editorialist Eggers received honoraria from Roche Diagnostics and Siemens Healthcare Diagnostics and has served as a consultant for Abbott Laboratories.

Reviewed by Zalman S. Agus, MD Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner